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Neurohormonal control of gastrointestinal blood flow

Mats Jodal, Ove Lundgren

10.1002/cphy.cp060146

Source: Supplement 16: Handbook of Physiology, The Gastrointestinal System, Motility and Circulation

Originally published: 1989

Published online: January 2011

Full Article on Wiley Online Library



Abstract

The sections in this article are:

1 Established Neurotransmitters
1.1 Acetylcholine
1.2 Norepinephrine
2 Neurotransmitter Candidates
2.1 Enkephalins
2.2 Neuropeptide Y
2.3 Peptide Histidine Isoleucine
2.4 Substance P
2.5 Vasoactive Intestinal Polypeptide
3 Hormones
3.1 Angiotensin
3.2 Antidiuretic Hormone
3.3 Epinephrine
3.4 Gastrin and Pentagastrin
3.5 Glucagon and Enteroglucagon
3.6 Secretin
4 Hormone Candidates
4.1 Motilin
4.2 Peptide YY
5 Neurotransmitters and/or Hormones
5.1 Cholecystokinin
5.2 5‐Hydroxytryptamine (Serotonin)
5.3 Neurotensin
5.4 Somatostatin
6 Integrated Responses
6.1 High‐Pressure Baroreceptors
6.2 Cardiac Mechanoreceptors
6.3 Arterial Chemoreceptors
6.4 Hemorrhagic Hypotension
6.5 Postprandial Hyperemia
Figure 1. Figure 1.

Effect of electrical field stimulation (single pulses, 2‐ms duration) on 3 different types of vascular smooth muscle preparations (upper panels) from rat. Experiments were performed in vitro, with tension measured between 2 metal rods introduced into vascular lumen. Electrical parameters were chosen so as to simulate only nervous tissue, as indicated by abolishment of response by tetrodotoxin. Lower panels, effect of single electrical pulses of long enough (100 ms) duration to stimulate directly vascular smooth muscles. Experiment was performed in presence of 0.1 μM tetrodotoxin in organ bath. Note large difference in nervous effects on different vessels.

From Nilsson 291
Figure 2. Figure 2.

A: responses of rat isolated small mesenteric artery and vein to exogenous norepinephrine (NA). B: corresponding responses to transmural electrical field stimulation at 16 Hz and supramaximal intensity of electrical stimulation. C: lack of responses to transmural field stimulation of type used in B after exposure to tetrodotoxin (TTX, 0.1 μM).

From Nilsson et al. 294
Figure 3. Figure 3.

Effect of electrical stimulation of splanchnic nerves (signal) on arterial pressure, tissue volume, intestinal blood flow, capillary filtration coefficient (CFC, Kf,c), and permeability‐surface area product (PS) for 86Rb in feline small intestine. PS values were determined at regular intervals as indicated on figure. CFC was estimated from slow, continuous increase of tissue volume while increasing venous outflow pressure. Blood flow was measured with drop counter coupled to ordinate writer, implying that ordinate height is inversely proportional to rate of blood flow. Note that vasoconstriction of veins (estimated from decrease of tissue volume) and precapillary sphincters (measured with CFC and PS) is maintained in the face of decreasing flow resistance.

From Dresel et al. 93
Figure 4. Figure 4.

Effect of electrical stimulation of periarterial nerves (signal) on venous outflow and on flow, volume, and mean transit time (tA/H) for plasma in villi. Experiment was performed in cat small intestine, and electrical stimulation was performed at 8 Hz, 10 V, 5 ms.

From Svanvik 389
Figure 5. Figure 5.

Hypothetical arrangements of nervous reflex underlying vasodilator response to mechanical stimulation of small intestine mucosa. Two possible mechanisms are presented. Left, reflex arrangement with mechanical receptor in tissue being activated, which in turn activates via serotonin (5‐HT) synapse a 2nd neuron releasing vasoactive intestinal polypeptide (VIP) at vascular smooth muscle cells. According to reflex arrangement on right, enterochromaffin (EC) cell acts as mechanoreceptor activating a VIPergic neuron. In the colon, reflex arrangements may be similar, although a cholinergic neuron may be included in reflex.
Figure 6. Figure 6.

Effects of reduction of pressure and pulsations in perfused right carotid sinus on resistance and capacitance vessels and net transcapillary fluid transfer in feline hindquarters and intestine. Cat was anesthetized with chloralose, curarized, atropinized, and kept under artificial ventilation. Vagal nerves had been cut in the neck. Intestinal blood flow was measured in such a way that height of ordinate writer was inversely proportional to rate of blood flow, whereas there was a direct relation between height and flow rate when recording hindquarter blood flow. Note continuous decrease in hindquarter volume on lowering carotid sinus pressure, whereas intestinal tissue volume after a transient decrease stays more or less constant. Peripheral resistance units (PRU) were calculated by dividing arterial pressure (in mmHg) by regional blood flow (in ml · 100 g−1 · min−1).

From Öberg 298
Figure 7. Figure 7.

Average response to lower body negative pressure (LBNP) of 9 subjects. MP, mean pressure; PP, pulse pressure; RAP, right atrial pressure; HR, heart rate; SBF, splanchnic blood flow; FBF, forearm blood flow. Broken line for aortic MP shows response of 2 subjects, who had a marked fall at LBNP of −35 mmHg; solid line thereafter shows average aortic MP for remaining 4 subjects. Asterisk denotes first 3 significant decrements (P < 0.05) in splanchnic blood flow beyond control.

From Johnson et al. 206
Figure 8. Figure 8.

Relative change of central blood volume (ΔCBV) as related to relative change of intestinal flow resistance (peripheral resistance units, ΔPRU) in cats. CBV was changed by positive pressure ventilation and estimated by an indicator‐dilution technique. Decrease of CBV is accompanied by increased PRU, probably reflecting decreased inhibition of bulbar vasopressor center through deloading of intrathoracic volume receptors.

From Sjövall et al. 381


Figure 1.

Effect of electrical field stimulation (single pulses, 2‐ms duration) on 3 different types of vascular smooth muscle preparations (upper panels) from rat. Experiments were performed in vitro, with tension measured between 2 metal rods introduced into vascular lumen. Electrical parameters were chosen so as to simulate only nervous tissue, as indicated by abolishment of response by tetrodotoxin. Lower panels, effect of single electrical pulses of long enough (100 ms) duration to stimulate directly vascular smooth muscles. Experiment was performed in presence of 0.1 μM tetrodotoxin in organ bath. Note large difference in nervous effects on different vessels.

From Nilsson 291


Figure 2.

A: responses of rat isolated small mesenteric artery and vein to exogenous norepinephrine (NA). B: corresponding responses to transmural electrical field stimulation at 16 Hz and supramaximal intensity of electrical stimulation. C: lack of responses to transmural field stimulation of type used in B after exposure to tetrodotoxin (TTX, 0.1 μM).

From Nilsson et al. 294


Figure 3.

Effect of electrical stimulation of splanchnic nerves (signal) on arterial pressure, tissue volume, intestinal blood flow, capillary filtration coefficient (CFC, Kf,c), and permeability‐surface area product (PS) for 86Rb in feline small intestine. PS values were determined at regular intervals as indicated on figure. CFC was estimated from slow, continuous increase of tissue volume while increasing venous outflow pressure. Blood flow was measured with drop counter coupled to ordinate writer, implying that ordinate height is inversely proportional to rate of blood flow. Note that vasoconstriction of veins (estimated from decrease of tissue volume) and precapillary sphincters (measured with CFC and PS) is maintained in the face of decreasing flow resistance.

From Dresel et al. 93


Figure 4.

Effect of electrical stimulation of periarterial nerves (signal) on venous outflow and on flow, volume, and mean transit time (tA/H) for plasma in villi. Experiment was performed in cat small intestine, and electrical stimulation was performed at 8 Hz, 10 V, 5 ms.

From Svanvik 389


Figure 5.

Hypothetical arrangements of nervous reflex underlying vasodilator response to mechanical stimulation of small intestine mucosa. Two possible mechanisms are presented. Left, reflex arrangement with mechanical receptor in tissue being activated, which in turn activates via serotonin (5‐HT) synapse a 2nd neuron releasing vasoactive intestinal polypeptide (VIP) at vascular smooth muscle cells. According to reflex arrangement on right, enterochromaffin (EC) cell acts as mechanoreceptor activating a VIPergic neuron. In the colon, reflex arrangements may be similar, although a cholinergic neuron may be included in reflex.



Figure 6.

Effects of reduction of pressure and pulsations in perfused right carotid sinus on resistance and capacitance vessels and net transcapillary fluid transfer in feline hindquarters and intestine. Cat was anesthetized with chloralose, curarized, atropinized, and kept under artificial ventilation. Vagal nerves had been cut in the neck. Intestinal blood flow was measured in such a way that height of ordinate writer was inversely proportional to rate of blood flow, whereas there was a direct relation between height and flow rate when recording hindquarter blood flow. Note continuous decrease in hindquarter volume on lowering carotid sinus pressure, whereas intestinal tissue volume after a transient decrease stays more or less constant. Peripheral resistance units (PRU) were calculated by dividing arterial pressure (in mmHg) by regional blood flow (in ml · 100 g−1 · min−1).

From Öberg 298


Figure 7.

Average response to lower body negative pressure (LBNP) of 9 subjects. MP, mean pressure; PP, pulse pressure; RAP, right atrial pressure; HR, heart rate; SBF, splanchnic blood flow; FBF, forearm blood flow. Broken line for aortic MP shows response of 2 subjects, who had a marked fall at LBNP of −35 mmHg; solid line thereafter shows average aortic MP for remaining 4 subjects. Asterisk denotes first 3 significant decrements (P < 0.05) in splanchnic blood flow beyond control.

From Johnson et al. 206


Figure 8.

Relative change of central blood volume (ΔCBV) as related to relative change of intestinal flow resistance (peripheral resistance units, ΔPRU) in cats. CBV was changed by positive pressure ventilation and estimated by an indicator‐dilution technique. Decrease of CBV is accompanied by increased PRU, probably reflecting decreased inhibition of bulbar vasopressor center through deloading of intrathoracic volume receptors.

From Sjövall et al. 381
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Article Title: Neurohormonal control of gastrointestinal blood flow
 

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Mats Jodal, Ove Lundgren. Neurohormonal control of gastrointestinal blood flow. Compr Physiol 2011, Supplement 16: Handbook of Physiology, The Gastrointestinal System, Motility and Circulation: 1667-1711. First published in print 1989. doi: 10.1002/cphy.cp060146